McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher exposes hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function
while leaving mitochondrial activity intact. Several hours
, later, the cells demonstrate reduced plasma protein
secretion and cytoplasmic swelling. Which mechanism
most directly explains these findings?
A. Impaired oxidative phosphorylation leading to ATP
depletion
B. Failure of ribosomal protein synthesis and defective
membrane trafficking
C. Activation of lysosomal hydrolases causing autophagy
D. Excessive microtubule polymerization interfering with
mitosis
Correct Answer: B
Rationale:
• Clinical Clue: Reduced plasma protein secretion strongly
implicates rough endoplasmic reticulum dysfunction.
• Mechanism: Ribosomes attached to rough ER synthesize
secretory and membrane proteins, which are subsequently
processed and trafficked through the Golgi apparatus.
• Why the Correct Answer Is Right: Loss of rough ER function
impairs synthesis and transport of proteins destined for
secretion, causing intracellular accumulation and osmotic
swelling.
• Why the Other Options Are Wrong:
o A: Mitochondrial oxidative phosphorylation remains
intact.
, o C: Lysosomal activation causes degradation, not
isolated secretory failure.
o D: Microtubules affect cell division and transport but
do not primarily explain protein synthesis failure.
• Exam Trap: Confusing rough ER dysfunction with
generalized ATP depletion.
• High-Yield Clinical Correlation: Plasma cells have abundant
rough ER because of intense immunoglobulin production.
• Memory Anchor: “Rough ER = Ribosome-rich protein
factory.”
Q2. A child with recurrent bacterial infections is found to
have defective neutrophil chemotaxis caused by impaired
actin filament assembly. Which cellular structure is most
directly affected?
A. Intermediate filaments
B. Microtubules
C. Microfilaments
D. Centrosomes
Correct Answer: C
Rationale:
• Clinical Clue: Chemotaxis and cellular movement depend
heavily on actin dynamics.
, • Mechanism: Microfilaments composed of actin regulate
cell shape, contraction, and motility.
• Why the Correct Answer Is Right: Defective actin
polymerization directly impairs pseudopod formation and
leukocyte migration.
• Why the Other Options Are Wrong:
o A: Intermediate filaments mainly provide structural
stability.
o B: Microtubules primarily mediate intracellular
transport and spindle formation.
o D: Centrosomes organize microtubules during mitosis.
• Exam Trap: Choosing microtubules because they also
participate in intracellular movement.
• High-Yield Clinical Correlation: Actin dysfunction
contributes to impaired wound healing and immune cell
migration disorders.
• Memory Anchor: “Actin drives action and movement.”
Q3. A pharmacologic agent inhibits the Na+/K+ ATPase
pump in myocardial cells. Which immediate
pathophysiologic change is most likely to occur?
A. Hyperpolarization of the plasma membrane
B. Increased intracellular sodium concentration
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher exposes hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function
while leaving mitochondrial activity intact. Several hours
, later, the cells demonstrate reduced plasma protein
secretion and cytoplasmic swelling. Which mechanism
most directly explains these findings?
A. Impaired oxidative phosphorylation leading to ATP
depletion
B. Failure of ribosomal protein synthesis and defective
membrane trafficking
C. Activation of lysosomal hydrolases causing autophagy
D. Excessive microtubule polymerization interfering with
mitosis
Correct Answer: B
Rationale:
• Clinical Clue: Reduced plasma protein secretion strongly
implicates rough endoplasmic reticulum dysfunction.
• Mechanism: Ribosomes attached to rough ER synthesize
secretory and membrane proteins, which are subsequently
processed and trafficked through the Golgi apparatus.
• Why the Correct Answer Is Right: Loss of rough ER function
impairs synthesis and transport of proteins destined for
secretion, causing intracellular accumulation and osmotic
swelling.
• Why the Other Options Are Wrong:
o A: Mitochondrial oxidative phosphorylation remains
intact.
, o C: Lysosomal activation causes degradation, not
isolated secretory failure.
o D: Microtubules affect cell division and transport but
do not primarily explain protein synthesis failure.
• Exam Trap: Confusing rough ER dysfunction with
generalized ATP depletion.
• High-Yield Clinical Correlation: Plasma cells have abundant
rough ER because of intense immunoglobulin production.
• Memory Anchor: “Rough ER = Ribosome-rich protein
factory.”
Q2. A child with recurrent bacterial infections is found to
have defective neutrophil chemotaxis caused by impaired
actin filament assembly. Which cellular structure is most
directly affected?
A. Intermediate filaments
B. Microtubules
C. Microfilaments
D. Centrosomes
Correct Answer: C
Rationale:
• Clinical Clue: Chemotaxis and cellular movement depend
heavily on actin dynamics.
, • Mechanism: Microfilaments composed of actin regulate
cell shape, contraction, and motility.
• Why the Correct Answer Is Right: Defective actin
polymerization directly impairs pseudopod formation and
leukocyte migration.
• Why the Other Options Are Wrong:
o A: Intermediate filaments mainly provide structural
stability.
o B: Microtubules primarily mediate intracellular
transport and spindle formation.
o D: Centrosomes organize microtubules during mitosis.
• Exam Trap: Choosing microtubules because they also
participate in intracellular movement.
• High-Yield Clinical Correlation: Actin dysfunction
contributes to impaired wound healing and immune cell
migration disorders.
• Memory Anchor: “Actin drives action and movement.”
Q3. A pharmacologic agent inhibits the Na+/K+ ATPase
pump in myocardial cells. Which immediate
pathophysiologic change is most likely to occur?
A. Hyperpolarization of the plasma membrane
B. Increased intracellular sodium concentration
